Inhibition of preovulatory gonadotropin secretion and stimulation of prolactin secretion by 7,12-dimethylbenz(a)anthracene in Sprague-Dawley rats.

Inhibition of preovulatory gonadotropin secretion and stimulation of prolactin secretion by 7,12-dimethylbenz(a)anthracene in Sprague-Dawley rats.
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7,12-二甲基苯并(a)蒽抑制 Sprague-Dawley 大鼠排卵前促性腺激素分泌并刺激催乳素分泌。

DOI:
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发表时间:
1979
期刊:
影响因子:
11.2
通讯作者:
A. E. Abed
A. E. Abed
中科院分区:
医学1区
文献类型:
--
作者:
Bernard Kerdelhué;A. E. Abed

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被引文献

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本文测定了DMBA敏感大鼠(Sprague-Dawley)和DMBA耐药大鼠(Wistar)在发情周期的特定时间点血清促黄体生成素、促卵泡激素、催乳素、促甲状腺激素和生长激素以及下丘脑促黄体生成素和促甲状腺激素的含量,直至DMBA敏感动物首次出现乳腺肿瘤。在DMBA处理后的第14 ~ 15个发情周期,肿瘤的发生率接近100%。通过使用两种品系的4天周期大鼠组进行激素测定,这些大鼠在出生后约55天的单次间情期I给予DMBA或溶媒(芝麻油)。在给药后第5和第11个发情周期的发情前期和发情期的上午和下午,在未预先麻醉的情况下,通过断头处死动物。在Sprague-Dawley雌性大鼠中,DMBA显著抑制促黄体生成素和促卵泡激素激增,并在处理后的任何发情周期的发情前期下午刺激催乳素激增(对于任何发情周期或处理,两种品系的排卵前激增时间相同);在发情周期的其他时间,未发现任何激素的差异。相比之下,Wistar大鼠没有表现出紊乱的排卵前或基础催乳素和促性腺激素的释放后,治疗与致癌物,此外,没有发现任何其他激素在任何时间测试的差异。这些结果表明,有一个特定的和短暂的激素失调,在DMBA-抗性品系的大鼠。由于激素失衡在整个诱导期内基本相同,因此DMBA治疗必然导致下丘脑垂体轴激素周期性相关中心的早期和持续改变。
Abstract Serum luteinizing hormone, follicle-stimulating hormone, prolactin, thyroid-stimulating hormone, and growth hormone and hypothalamic luliberin and thyroliberin contents were measured at given times of the estrous cycle in a dimethylbenz( a )anthracene (DMBA)-susceptible strain of rat (Sprague-Dawley) and in a DMBA-resistant strain of rat (Wistar) for periods up to the appearance of the first mammary tumors in DMBA-susceptible animals. Tumors usually appeared with ≃100% incidence around the 14th to 15th estrous cycle after DMBA treatment in Sprague-Dawley rats. Hormonal determinations were done by using groups of 4-day cycling rats of both strains which were given DMBA or the vehicle (sesame oil) on a single diestrus I at around 55 days of life. Animals were sacrificed by decapitation without previous anesthesia on the morning and afternoon of proestrus and estrus during the 5th and 11th estrous cycles after treatment. In Sprague-Dawley female rats, DMBA significantly inhibited luteinizing hormone and follicle-stimulating hormone surges and stimulated the prolactin surge on the afternoon of proestrus at any estrous cycle after treatment (the timing of preovulatory surges was the same in both strains for any estrous cycle or treatment); no difference was found for any hormone at other times of the estrous cycle. In contrast, Wistar rats did not show deranged preovulatory or basal prolactin and gonadotropin release after treatment with the carcinogen; in addition, no difference was found for any other hormone at any time tested. These results show that there is a specific and transient hormonal deregulation in a DMBA-susceptive strain of rats. Inasmuch as the hormonal imbalance was essentially the same throughout the induction period, an early and persistent alteration in centers implicated in the hormonal cyclicity of the hypothalamopituitary axis must result from DMBA treatment.